Dr. Petit Patrice X.,

PX Petit completed University studies at the University of Paris Pierre et Marie Curie in France (Doctor es Sciences, 1984) and earned a Ph.D. in biology from the University Paris 7 Paris-Diderot in 1979. Early in his career, PX Petit worked for the National Center for Scientific Research, CNRS, France and worked on lichen physiology and adaptation to cold (He sejouned in Norway and Germany during this time for collaboration). He switched later for the study of plant mitochondria (C3, C4 and CAM plants) at the Univerity Pierre et Marie Curie. That was the occasion to spend two year in Sweden working on the characteristic of the mitochondrial membranes (Umea and Lund) before moving to the CNRS center in Gif-sur-Yvette, France where he establised the first flow cytometry department devoided only on plant cell studies (together with Spencer Craig Brown and Catherine Bergounioux. Then switching to the animal field, PX Petit first discovered the fact that mitochondrial membrane permeabilization is a concrete step in the process of programmed cell death (1994 - 1996) with his work realized with different teams (B. Mignotte, Gif-sur-Yvette - ML Gougeon, Institut Pasteur and G. Kroemer, IRC Villejuif). Since this date, he worked on The role of Bcl-2 proteins members in the induction of apoptosis (original Work on Bid) and to the role of caspase-8 (Institut Cochin). Paris. Now in another laboratory he shifted to somes aspect of toxicology concerning the role of pollutant mixtures in the cellular behaviour and also started to work on polyphenols (curcumin and resveratrol), trying to follow their hormetic effects.

Research Interest

Central mechanisms of apoptosis linked to mitochondria in cancer and human pathologies with a special dedication to cardiolipin dysmetabomism (i.e., rare diseases like the « Barth syndrome »).
Study of the Bcl-2 family member Bid in its interactions with mitochondrial membrane and membrane « mimetic » systems like giant unilamellar vesicles.
Toxicology : role of polyphenol in apoptosis and autophagy